Aims, methods and expected results; 1. To complete the behavioural phenotype characterization of 3xTgAD mice (non-3xTgAD) used as control group and to study new neurochemical/molecular correlates (....). we expect that the pathological spectrum described for 3xTgAD mice find its correlate with deficits in learning and memory and altered non-cognitive aspects (BPSD: sundowning behaviour, anxiety) and also at neurochemical/biological level with decrease of sulfatides, changes in polyamines, NMDA receptors and synaptic plasticity, characteristics of this disease. 2. We'll study the preventive and therapeutic effects of cognitive stimulation (handling and environmental enrichment) in this animal model at early and advances stages of the disease and from three levels of study: behavioural (cognitive deficits and BPSD), neuropathological (intra and extracellular \betaamiloid; tangles of tau) and at neurochemical/molecular level (NMDA, muscarinic and nicotinic receptors autoradiography, polyamines system and pCREB, BDNF, NGF immunohystochemistry; 2D electroforesis of synaptic proteins and TOF-SIMS of sulfatides). We expect that both treatments have beneficial effects at the behavioural level and be also able to modify in the areas diana of the disease (...) neuronal processes associated to the neuropathology of Alzheimer's disease: rescuing cholinergic and NMDA receptors, reducing the decrease of sulfatides, increasing neurotrofins and restablishing polyamines and synaptic proteins composition/levels.
|Effective start/end date||1/10/06 → 30/09/09|